This study describes a noninvasive method for detecting delayed ventricular activation, caused by ischemia, on the body surface. Signal averaging and a newly developed high-pass digital filter were used. The filter has the property that it does not create an artifact or ring after the QRS complex ends, thereby allowing the detection of microvolt-level potentials that occur immediately after the QRS complex. Eleven dogs were studied before and during acute ischemia induced by coronary artery ligation and latex embolization. The ischemic region was mapped with bipolar electrodes and, after the chest was rapidly closed, signal-averaged recordings were made from the body surface. Repeated cycles of ventricular mapping and signal averaging were performed. In each dog, delayed and fractionated electrograms were recorded directly from the ischemic epicardium that lasted a maximum of 118 +/- 18 ms after QRS onset. The duration of the ventricular electrograms varied with time. Whenever delayed epicardial electrograms were recorded, filtered signal-averaged leads showed microvolt-level potentials early in the S-T segment that were continuous with the QRS complex. The duration of ventricular activation, as measured from the bipolar electrograms and from the filtered signal-averaged leads, correlated well (r = 0.93, P less than 0.001). Because of the absence of filter ringing, low-level potentials could be detected less than 40 ms after the QRS complex ended. This study demonstrates that microvolt-level potentials arising from delayed ventricular activation can be reliably detected on the body surface, even when they occur just after the QRS complex.
Usefulness and limitation of the body surface VAT (ventricular activation time) isochrone mapping for inferring the excitation spread disorders in the ventricles
